Myocardial necrosis as assessed by cardiac troponin elevation occurs frequently after coronary stenting and is associated with adverse clinical outcome. Mechanical factors have been implicated in this complication and the role of systemic inflammation is not known.

We prospectively studied 208 patients with chronic stable angina who underwent elective coronary stenting. All patients had normal troponin levels before the procedure. Blood samples for high-sensitivity C-reactive protein (CRP) were obtained before the procedure and analyzed using a high-sensitivity kit. Cardiac troponin T (cTnT) was obtained 24 hours after the procedure.

Postprocedural cTnT elevations were observed in 46 (22%) patients. There were 11 (16%), 14 (20%), and 21 (30%) patients with elevated postprocedural cTnT in the first, second, and third CRP tertile, respectively (P for trend = .045). In a multivariate logistic regression model, adjusting for all the significant univariate predictors and for statin therapy, CRP remained a significant independent predictor of postprocedural cTnT elevation with an odds ratio of 2.6 in patients in the third CRP tertile compared with patients in the first CRP tertile (95% CI 1.1-6.0, P = .02). Patients in the third CRP tertile also had higher cTnT elevations compared with patients in the first and second CRP tertile (P = .03).

Elevated baseline CRP levels are associated with higher risk of postprocedural troponin elevations in patients with stable angina undergoing uncomplicated coronary stenting. These results underscore the role of systemic inflammation in the pathogenesis of periprocedural myocardial injury.